Hexavalent chromium (Cr(VI)) compounds are widely found in different working environments. These compounds can cause apoptosis in human cells, but the mechanisms underlying chromium-induced apoptosis are not clear. A marker of apoptosis is the exposure of phosphatidylserine on cell membrane and the modification of phosphatidylserine metabolism. The aim of this study was to verify whether chromium could cause phosphatidylserine exposure and modification of its metabolism in human lymphoblastic leukemia cell line (MOLT-4). METHODS: Phosphatidylserine exposure was evaluated by annexin V binding whereas phosphatidylserine metabolism was studied measuring the incorporation of [³H]serine. RESULTS: Cell treatment with Cr(VI) increases phosphatidylserine exposure and cell apoptosis, but decreases the incorporation of [³H]serine into phosphatidylserine in a dose- and time-dependent manner. CONCLUSIONS: The Cr(VI)-induced apoptosis also through modification of phosphatidylserine exposure and metabolism.

Phosphatidylserine metabolism in human lymphoblastic cells exposed to chromium (VI).

GAMBELUNGHE, Angela;BURATTA, Sandra;FERRARA, GIUSEPPINA;MOZZI, Rita;MARCHETTI, Maria Cristina;MURGIA, Nicola;MUZI, Giacomo
2011

Abstract

Hexavalent chromium (Cr(VI)) compounds are widely found in different working environments. These compounds can cause apoptosis in human cells, but the mechanisms underlying chromium-induced apoptosis are not clear. A marker of apoptosis is the exposure of phosphatidylserine on cell membrane and the modification of phosphatidylserine metabolism. The aim of this study was to verify whether chromium could cause phosphatidylserine exposure and modification of its metabolism in human lymphoblastic leukemia cell line (MOLT-4). METHODS: Phosphatidylserine exposure was evaluated by annexin V binding whereas phosphatidylserine metabolism was studied measuring the incorporation of [³H]serine. RESULTS: Cell treatment with Cr(VI) increases phosphatidylserine exposure and cell apoptosis, but decreases the incorporation of [³H]serine into phosphatidylserine in a dose- and time-dependent manner. CONCLUSIONS: The Cr(VI)-induced apoptosis also through modification of phosphatidylserine exposure and metabolism.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11391/1038518
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